Xin Fu Kang oral liquid inhibits excessive myocardial mitophagy in a rat model of advanced heart failure

Heart failure caused by myocardial infarction is a common cardiovascular disease with high mortality rate. Myocardial mitophagy is involved in the process of occurrence and development of heart failure. In this study, we aimed to investigate the effects of Xin Fu Kang (XFK) oral liquid on myocardial mitophagy in a rat model of advanced heart failure. The rat model of advanced heart failure was established by ligating the left anterior descending (LAD) artery for eight weeks. Captopril and XFK were given by gavage separately. Cardiac function and myocardial mitochondrial ultrastructure were observed. Co-localization of mitophagy-related proteins was observed by fluorescence microscopy. Quantitative polymerase chain reaction (qPCR) and western blotting were performed for mRNA and protein level detection, respectively. Compared with the sham group, advanced heart failure group showed a significant reduction in cardiac function with destruction of myocardial mitochondrial structure. Co-localization between mitophagy-related proteins (parkin, p62, and LC3) and mitochondria increased significantly. The mRNA and protein levels of pink1, parkin, p62, and LC3 indicated that excessive mitophagy was observed in the rat model of advanced heart failure. XFK intervention could regulate pink/parkin pathway and inhibit excessive mitophagy.